Clinical differential diagnosis of parkinsonism

A complete history remains critical in establishing the correct diagnosis. The physician must inquire about medications, possible environmental exposures, and family history of neurological disease, including essential tremor, dominantly inherited spinal cerebellar ataxias, and dementia, as well as parkinsonism. Parkinsonism in the adolescent or young adult should never be assumed to be idiopathic PD until other causes have been ruled out. If the clinical features resemble PD in all respects and there is an affected sibling, than there is a good possibility that disease is caused by recessive mutations in the parkin gene. The absence of rest tremor makes the diagnosis of PD difficult. If the patient also failures to response to L Dopa, the diagnosis is in serious doubt. Patients should be reexamined with a close look for down-gaze paresis and facial dystonia (PSP), also static hypotension (MSA), bulbar dysfunction with truncal ataxia (MSA, SCA). Although postural instability is one of the cardinal features of PD, it is usually not prominent early in disease. When initial signs include postural instability out of proportion to other manifestations, the clinicians should look hard for other forms of parkinsonism. In particular, several parkinsonism-plus syndromes can present with postural instability in gait disorder, including PSP and MSA. Dementia at the onset of illness agues against PD, suggesting instead primary dementia with parkinsonian features. Forms of dementia with parkinsonian features include diffuse Lewy-body disease and Creutzfeldt-Jakob disease. Early cognitive changes are also common in PSP, which may misdiagnosed as Alzheimer's disease. Diffuse Lewy-body disease was until recently an underdiagnosed cause of dementia with parkinsonism, accounting for up to 20% of all dementia in the elderly. Although usually unilateral in onset, PD typically becomes bilateral within several years. A patient whose disease persists in a markedly asymmetric manner may have corticobasal degeneration or hemiparkinsonism-hemiatrophy. Clinical differential diagnosis can often be made easier by SPECT, PET, smelling tests, and brain parenchyma sonography, nevertheless history and results of neurological examination are still crucial in establishing the cause of parkinsonism.